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Eating Wild Deer Can Cause Chronic Wasting Disease (CWD)

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Mar 2, 2005
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Eating wild deer unsafe
By John Soltes
Jan 27, 2006, 19:46

Deer and elk that are infected with mad cow-like disease, known as chronic wasting disease (CWD), carry infectious agents called prions in their leg muscles, indicating that those handling and eating infected deer meat may contract the same disease, University of Kentucky researchers reported on Jan. 26 in The Journal Science.

This newfound evidence is shocking because the public has been informed that the infectious prion protein for CWD was only present in parts of the nervous system such as brains and backbones. It was thought in the past that only nervous tissues from infected deer were susceptible to spreading the disease.

Previous studies found that mice injected with brain tissue from infected deer get brain wasting disease, indicating that nervous systems are the risky material. The current finding shows that eating infected deer muscles can also be a way for the disease to spread to humans.

In the study, mice injected with extracts from leg muscles of deer infected with chronic wasting disease were found to suffer the same disease, proving that the infectious prions are present in leg muscles, not just nervous tissues.

Glenn Telling, the lead researcher from the University of Kentucky, said that these findings may prove venison can carry chronic wasting disease to humans.

"We don't know how the infectious prion goes from the central nervous system into the muscle," Telling was quoted as saying by Newsday.

"But it raises the possibility that hunters could be exposed to prions by consuming or handling (deer) meat."

Chronic wasting disease is a serious disease that has affected deer and elk throughout North America. It has already been found in both wild and captive deer and elk in many states including Colorado, Illinois, Kansas, Minnesota, Montana, Nebraska, New Mexico, Oklahoma, South Dakota, Utah, Wisconsin, New York, Wyoming, and West Virginia.

The finding will raise much concern about meatpackers and hunters that continually deal with venison meat. In addition, the muscle part of the deer is commonly used in food meals and dishes.

"Anybody who may be handling or eating infected deer may be inadvertently exposed," Telling was quoted as saying to the Milwaukee Journal Sentinel.

Last year, chronic wasting disease was found in captive deer in New York. The state officials said that no evidence indicates humans get brain wasting disease by eating infected deer meat. The current study is expected to affect the government's advisories on deer meat consumption.

State officials, namely Wisconsin Department of Health's epidemiologist James Kazmierczak, are stating that nothing new has to be done to avoid the spread of the chronic wasting disease. They now call for the destruction of any animal carrying the disease, whether the infection is in the brain or leg muscle although these special precautions might not be taken seriously by everyone, according to Kazmierczak.

It is known that people who consume beef from cattle infected with bovine spongiform encephalopathy (BSE) can get the human form ma d c ow disease called variant Creutzfeldt-Jakob disease or vCJD, which have victimized more than 100 people worldwide.

The new evidence suggests the transmission may not be necessary because the meat is tainted with the risky material such as brain tissue, but because the meat may contain infectious agents.

However, that turns out not to be true. One of the alarming characteristics of m ad cow disease is that prions are not found in the leg muscle.

So far, it has not been unclear where the deer chronic wasting disease comes from. It may be a result of spontaneity or transmitted from other animals. If the latter holds true, the prion may be changing when it makes the jump from animal-to-animal

The Associated Press reported that Judd Aiken, a prion researcher at the University of Wisconsin, believes that no one should eat venison from areas that are suspected of infection. He believes that this precaution should be practiced even in areas where negative tests have come about.

However, the real risk may not be as it appears to be. Chronic wasting disease does not transmit into mice with human prions, indicating that humans may be more resistant to the disease, the New York Times cited Dr. Telling as saying. Also oral transmission of the prion protein is less efficient than injecting prions into the brain.

The transmissible spongiform encephalopathy (TSE) agents or prions are extremely resistant to heat, ultraviolet light, ionizing radiation, normal sterilization processes, and common disinfectants that normally inactivate viruses and bacteria, according to United States Department of Agriculture. No one should expect that ordinary cooking methods kill the agents.


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Mar 2, 2005
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The new evidence suggests the transmission may not be necessary because the meat is tainted with the risky material such as brain tissue, but because the meat may contain infectious agents.

((((However, that turns out not to be true. One of the alarming characteristics of mad cow disease is that prions are not found in the leg muscle. ))))NOT,I think they need to go back to school and start over!!!!!!


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Feb 11, 2005
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Home on the Range, Alberta
They don't need to start ALL over, just start over from a different perspective:

Health Phys. 2005 May;88(5):423-38. Related Articles, Links

Radionuclides and trace metals in Canadian moose near uranium mines: comparison of radiation doses and food chain transfer with cattle and caribou.
Thomas P, Irvine J, Lyster J, Beaulieu R.

Toxicology Centre, University of Saskatchewan, 44 Campus Drive, Saskatoon, Saskatchewan S7N 5B3 Canada. [email protected]

Tissues from 45 moose and 4 cattle were collected to assess the health of country foods near uranium mines in northern Saskatchewan. Bone, liver, kidney, muscle and rumen contents were analyzed for uranium, radium-226 (226Ra), lead-210 (210Pb), and polonium-210 (210Po). Cesium-137 (137Cs), potassium-40 (40K), and 27 trace metals were also measured in some tissues. Within the most active mining area, Po in liver and muscle declined significantly with distance from tailings, possibly influenced by nearby natural uranium outcrops. Moose from this area had significantly higher 226Ra, 210Pb, 210Po, and 137Cs in some edible soft tissues vs. one control area. However, soil type and diet may influence concentrations as much as uranium mining activities, given that a) liver levels of uranium, 226Ra, and 210Po were similar to a second positive control area with mineral-rich shale hills and b) 210Po was higher in cattle kidneys than in all moose. Enhanced food chain transfer from rumen contents to liver was found for selenium in the main mining area and for copper, molybdenum and cadmium in moose vs. cattle. Although radiological doses to moose in the main mining area were 2.6 times higher than doses to control moose or cattle, low moose intakes yielded low human doses (0.0068 mSv y(-1)), a mere 0.3% of the dose from intake of caribou (2.4 mSv y(-1)), the dietary staple in the area.

PMID: 15824592 [PubMed - indexed for MEDLINE]

Environ Health Perspect. 1999 Jul;107(7):527-37. Related Articles, Links

Radionuclides in the lichen-caribou-human food chain near uranium mining operations in northern Saskatchewan, Canada.

Thomas PA, Gates TE.

Toxicology Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. [email protected]

The richest uranium ore bodies ever discovered (Cigar Lake and McArthur River) are presently under development in northeastern Saskatchewan. This subarctic region is also home to several operating uranium mines and aboriginal communities, partly dependent upon caribou for subsistence. Because of concerns over mining impacts and the efficient transfer of airborne radionuclides through the lichen-caribou-human food chain, radionuclides were analyzed in tissues from 18 barren-ground caribou (Rangifer tarandus groenlandicus). Radionuclides included uranium (U), radium (226Ra), lead (210Pb), and polonium (210Po) from the uranium decay series; the fission product (137Cs) from fallout; and naturally occurring potassium (40K). Natural background radiation doses average 2-4 mSv/year from cosmic rays, external gamma rays, radon inhalation, and ingestion of food items. The ingestion of 210Po and 137Cs when caribou are consumed adds to these background doses. The dose increment was 0.85 mSv/year for adults who consumed 100 g of caribou meat per day and up to 1.7 mSv/year if one liver and 10 kidneys per year were also consumed. We discuss the cancer risk from these doses. Concentration ratios (CRs), relating caribou tissues to lichens or rumen (stomach) contents, were calculated to estimate food chain transfer. The CRs for caribou muscle ranged from 1 to 16% for U, 6 to 25% for 226Ra, 1 to 2% for 210Pb, 6 to 26% for 210Po, 260 to 370% for 137Cs, and 76 to 130% for 40K, with 137Cs biomagnifying by a factor of 3-4. These CRs are useful in predicting caribou meat concentrations from the lichens, measured in monitoring programs, for the future evaluation of uranium mining impacts on this critical food chain.

PMID: 10378999 [PubMed - indexed for MEDLINE]

J Environ Radioact. 2002;63(2):153-71. Related Articles, Links

Distribution of long-lived radionuclides of the 238U series in the sediments of a small river in a uranium mineralized region of Spain.
Lozano JC, Blanco Rodriguez P, Tome FV.

Laboratorio de Radiactividad Ambiental, Facultad de Ciencias, Universidad de Salamanca, Spain.

A study is presented on the distribution and mobilization of the natural U isotopes (238U and 234U), 230Th, and 226Ra in the sediments of a small river crossing an uranium mineralized zone where a disused uranium mine is located. Due to the preferential directions for surface run-off waters and to the mine's situation, one sampling point along the river bed was identified as a point of accumulation of radionuclides. The average values of the activity concentrations (Bq/kg) in this sediment sample were 5,025, 5,055, 5,915 and 1,694 for 238U, 234U, 230Th and 226Ra, respectively, while the respective average values of the activity concentrations (Bq/kg) for the sediment sample considered to give the background level were 125, 124, 131 and 370. Isotopic ratios between the descendants of 238U served to clarify some paths of distribution, involving the soils nearest to the sampling points and the location of these points with respect to the disused mine. The differences in behaviour found between the uranium, thorium and radium isotopes were associated to the mobility of these radionuclides in the fluvial system studied. Correlations between the radionuclide activity concentration ratios and stable element concentrations in the sediment samples were also investigated.

PMID: 12363268 [PubMed - indexed for MEDLINE]

Radiat Prot Dosimetry. 2001;93(2):151-9. Related Articles, Links

210Pb, 210Po, 226Ra, U and Th in arable crops and ovine liver: variations in concentrations in the United Kingdom and resultant doses.

Ham GJ, Wilkins BT, Ewers LW.

National Radiological Protection Board, Chilton, Didcot, Oxon OX11 0RQ, UK.

Concentrations of a range of naturally occurring radionuclides have been determined in the same crops grown at two sites in the UK. Ovine liver has also been studied. One site was in an area where concentrations in soil are typical of the UK (the 'control' site) and the other in an area where levels were well above average (the 'test' site). For an average adult consumer of all of the foodstuffs studied, the doses from consumption for the test site were about 4 times higher than those for the control site. However, the differences were small compared with the variability in overall doses from natural background across the UK. 210Pb and 210Po were important contributors to doses for both sites, but at the test site the contribution from 226Ra was also significant. Of the foodstuffs studied, consumption of leafy vegetables and liver gave the highest doses. The doses from leafy vegetables were sensitive to the weather conditions prior to harvesting. Consequently, rigorous monitoring programmes should be based on several samples collected throughout the year; extrapolations based on a single annual sample are unlikely to be reliable.

PMID: 11548338 [PubMed - indexed for MEDLINE]

Sci Total Environ. 2001 Jun 12;273(1-3):163-9. Related Articles, Links

Daily intakes of 238U, 234U, 232Th, 230Th, 228Th and 226Ra in the adult population of central Poland.
Pietrzak-Flis Z, Rosiak L, Suplinska MM, Chrzanowski E, Dembinska S.

Central Laboratory for Radiological Protection, Warsaw, Poland. [email protected]

Activity concentration of the uranium and thorium series radionuclides was determined in foodstuffs and drinking water in central Poland. Annual and daily intake for the adult population was estimated from the concentrations determined and average annual consumption of food and water. The daily intakes (in mBq) were 22.1 (238U), 26.5 (234U), 2.38 (232Th), 4.06 (230Th), 11.2 (228Th) and 42.2 (226Ra). The intake of uranium isotopes occurred mainly with water; the main intake of thorium isotopes was with animal products, vegetables, cereals and potatoes, whereas 226Ra entered mainly with animal products, cereals and vegetables. From the intake and dose coefficients, the annual effective doses for the ingested radionuclides were calculated. The annual effective dose was 5.95 microSv, of which 72.4% originated from 226Ra.

PMID: 11419599 [PubMed - indexed for MEDLINE]

Sci Total Environ. 1989 Sep;85:119-28. Related Articles, Links

Influence of husbandry on the transfer of radiocaesium from feed to milk during the winter that followed the Chernobyl reactor accident.
Bradley EJ, Wilkins BT.

National Radiological Protection Board, Didcot, Oxon, United Kingdom.

The release of activity from the Chernobyl nuclear reactor resulted in deposition of radionuclides throughout the UK in early May 1986. Since that time, the transfer of radiocaesium from feed to milk has been followed at two farms that differ in both location and husbandry practice. This paper concerns the winter of 1986/87, when activity concentrations in milk increased because of the consumption of silage prepared earlier in the year. Silage-to-milk transfer coefficients have been estimated which suggest that, when incorporated into prepared silage, radiocaesium from Chernobyl is less available for transfer to cows' milk than soluble caesium-134 applied directly onto pasture. The measured activity concentrations in milk have been compared with those predicted by the NRPB model FARMLAND; despite differences between the husbandry practice assumed in the model and those observed in practice, the model provides an adequate radiological assessment of the feed-cow-milk pathway after an accidental release of radioactivity.

PMID: 2814439 [PubMed - indexed for MEDLINE]

Sci Total Environ. 1995 Dec 1;173-174:151-8. Related Articles, Links

Investigations of the potential bioavailability of 210Po in some foodstuffs.

Bulman RA, Ewers LW, Matsumoto K.

National Radiological Protection Board, Chilton, Didcot, England.

Extraction of 210Po from lamb's liver, pig's kidneys, mussel flesh and brown crabmeat with a series of solvent systems has been used to gain some insight into the uncertainty about the gastrointestinal absorption factor for Po incorporated into foodstuffs. By extracting the tissues with diethyldithiocarbamate dissolved in chloroform, and also in methanol, it has been shown that 210Po is more effectively extracted from lamb's liver and crabmeat than it is from each of the other tissues. A similar pattern of extractability is also evident for aqueous solutions of citric acid on crabmeat and mussel flesh. Of particular note is the low extractability by dimethylsulphoxide (3%) of 210Po in mussel flesh as opposed to 24% extractability of 210Po from crabmeat. 210Po-binding macromolecules of about 10 kDa have been released from crabmeat and mussel flesh by digestion with pepsin.

PMID: 8560221 [PubMed - indexed for MEDLINE]


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Feb 11, 2005
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Home on the Range, Alberta
J Toxicol Environ Health B Crit Rev. 2006 Jan-Feb;9(1):63-85. Related Articles, Links

The speciation of metals in mammals influences their toxicokinetics and toxicodynamics and therefore human health risk assessment(1).

Yokel RA, Lasley SM, Dorman DC.

Pharmaceutical Sciences, College of Pharmacy, and Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington, KY, 40536-0082, USA.

Chemical form (i.e., species) can influence metal toxicokinetics and toxicodynamics and should be considered to improve human health risk assessment. Factors that influence metal speciation (and examples) include: (1) carrier-mediated processes for specific metal species (arsenic, chromium, lead and manganese), (2) valence state (arsenic, chromium, manganese and mercury), (3) particle size (lead and manganese), (4) the nature of metal binding ligands (aluminum, arsenic, chromium, lead, and manganese), (5) whether the metal is an organic versus inorganic species (arsenic, lead, and mercury), and (6) biotransformation of metal species (aluminum, arsenic, chromium, lead, manganese and mercury). The influence of speciation on metal toxicokinetics and toxicodynamics in mammals, and therefore the adverse effects of metals, is reviewed to illustrate how the physicochemical characteristics of metals and their handling in the body (toxicokinetics) can influence toxicity (toxicodynamics). Generalizing from mercury, arsenic, lead, aluminum, chromium, and manganese, it is clear that metal speciation influences mammalian toxicity. Methods used in aquatic toxicology to predict the interaction among metal speciation, uptake, and toxicity are evaluated. A classification system is presented to show that the chemical nature of the metal can predict metal ion toxicokinetics and toxicodynamics. Essential metals, such as iron, are considered. These metals produce low oral toxicity under most exposure conditions but become toxic when biological processes that utilize or transport them are overwhelmed, or bypassed. Risk assessments for essential and nonessential metals should consider toxicokinetic and toxicodynamic factors in setting exposure standards. Because speciation can influence a metal's fate and toxicity, different exposure standards should be established for different metal species. Many examples are provided which consider metal essentiality and toxicity and that illustrate how consideration of metal speciation can improve the risk assessment process. More examples are available at a website established as a repository for summaries of the literature on how the speciation of metals affects their toxicokinetics.

PMID: 16393870 [PubMed - in process]


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Sep 3, 2005
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##################### Bovine Spongiform Encephalopathy #####################

Subject: Recent death may be Creutzfeldt-Jakob Disease Fort Collins Colorado
Date: January 28, 2006 at 7:53 am PST

Fort Collins Coloradoan
Article published Jan 27, 2006

Recent death may be Creutzfeldt-Jakob
Biopsy will tell if brain-wasting disease is to blame

[email protected]

The brain of a Fort Collins woman who died earlier this week will be tested
for Creutzfeldt-Jakob disease, a rare brain-wasting disease, a state
official confirmed.

Nancy Banks, 69, died Monday, just two months after suffering stroke-like
symptoms that her neurologist later determined to be CJD, according to her

Colorado has had 39 cases of CJD since the state began monitoring the
disease in 1998 - an average of 4.9 cases a year, said John Pape, the state
epidemiologist. Banks is the second person to be tested this year for the

"We've had a couple listed as CJD on the death certificate but turn out not
to be (CJD) at the autopsy," Pape said.

An autopsy or brain biopsy is the only way to confirm a CJD diagnosis,
though not all the cases counted by the state had autopsies, Pape said.
Tests also can identify the type of CJD: sporadic, hereditary, acquired or

There is no treatment or cure for the disease, and about 90 percent of
people with the disease die within a year, according to the National
Institute of Health's National Institute of Neurological Disorders and
Stroke. CJD causes memory failures, behavioral changes, coordination and
vision problems, according to the institute. It can also cause mental
deterioration, involuntary movement, blindness, weakness and coma as it

The average person stricken with classic CJD is 68 years old and lives four
to five months after symptoms set in, according to the U.S. Centers for
Disease Control and Prevention.

CJD belongs to a group of diseases called transmissible spongiform
encephalopathies that includes chronic wasting disease in deer and elk,
scrapie in sheep and bovine spongiform encephalopathy, or mad cow disease,
in cattle. The diseases are caused by abnormal proteins called prions.

About 93 percent of the 1,133 CJD cases in the U.S. since 1997 have been
sporadic or hereditary, according to a Coloradoan analysis of CJD
surveillance by the National Prion Disease Pathology Surveillance Center at
Case Western Reserve University in Cleveland.

"About 90 percent of CJD cases are sporadic," said Dr. Patrick Bosque, a
neurologist and prion researcher at Denver Health Medical Center. "The one
concern in Colorado is, could it be related to deer?"

Just one person in the U.S. has died from vCJD, and that person likely
acquired the disease in the United Kingdom, according to the surveillance
center. Colorado never has had a verified vCJD case, Pape said.

Nearly 160 people worldwide, most from the United Kingdom, are known to have
contracted the variant type of the disease after they ate beef from cattle
with mad cow disease.

Banks, born in Denver, spent nearly two decades as head of the Library and
Media Center of Riffenburgh Elementary School before moving to the LINC
Library, a summer reading program of the Fort Collins Library and the Poudre
School District, according to the obituary. She also started a library at
First Christian Church.

Samples collected from Banks will be sent to the National Prion Disease
Pathology Surveillance Center. It could be several months before results are
available, Pape said.

Pape declined to say who was collecting the samples from Banks. He said it's
difficult to find coroners or physicians willing to do autopsies on
potential CJD victims because there's a small risk of catching the disease
if infected material comes in contact with an open cut or orifice.

"There's some concern with autopsies and contamination and exposure," Pape
said. "A lot of coroners and hospitals absolutely will not do them."

Though the disease is rare, Pape said he believes awareness is "heightened"
among the neurologists he's talked to in the state.

"There are some hallmarks that can clue in a neurologist," Pape said.

When contacted by the Coloradoan, Banks' daughter, Afton Rorvik, said it was
too difficult at this time to talk about her mother's illness and death.


Nancy Banks
Born in Denver, CO
Departed on Jan. 23, 2006 and resided in Fort Collins, CO.

Memorial Service: Saturday Jan. 28, 2006
Cemetery: Private
Please click on the links above for locations, times, maps, and directions.

Knitting. Nancy Banks knitted in the dark, at meetings, on the telephone, during movies. As she drove down the highway in her silver Honda civic, her thumbs and forefingers sometimes twitched up and down, as if she were impatient to get back to whatever important project she was creating. Yarn and cloth bags containing various knitting projects could be found all over her house.

Born in 1936, in post-depression Denver, Colorado, Nancy’s mother taught her the rudiments of knitting at the age of five. Like most other things, Nancy approached knitting with energy, confidence, and a totally unique, self-taught approach. Sweaters for children, decorated blankets for married couples and grandchildren, baby booties and hats, crazy striped socks, scarves, and Christmas ornaments poured off her needles in a constant stream.

Nancy also understood and loved the written word. At her high school, the Kent school for girls, she edited the yearbook, and went on to Smith College, where she majored in German literature (after a brief flirtation with physics!) Her love of books led her to a Masters of Library Science from the University of Denver in 1973, and she headed the Library and Media Center of Riffenburgh Elementary School shortly after graduating.

In addition to repairing audio-visual equipment, and keeping the large collection of books, materials and computer equipment in order, Nancy understood her role as a caregiver, and a mentor. She loved making the library a safe, loving place for children. She brought her huge stuffed Gorilla named “George” to her story hour for them to hold, held programming classes, and helped a group of interested young students start a “Tolkien” group, exploring the world and mythologies of the author of “The Lord of the Rings.”

After retiring from Riffenburgh almost 10 years ago, Nancy went to work on the LINC program, a summer reading program that meshed resources and personnel from both the Fort Collins Public Library and the Poudre R1 School District. Her years in the schools helped her create a program that enabled families to come to events hosted at their local school library over the summer, and encouraged them and their children to read. The LINC programs, offered by members of the Fort Collins community, often followed her own broad interests: opera, dog-sledding, physics, and of course knitting.

During the time she could spare from the LINC program, Nancy traveled widely. Her favorite international places included Germany (where she had spent a year studying in 1958), England, Ireland and Wales (where she vividly remembered hearing of the September 11 tragedy.) She also regularly visited her close friends and family all over the United States, especially prioritizing spending time with her six grandchildren. Equally at home in the car or the airport, she only became anxious when airport security once confiscated her knitting needles, apparently deciding that this tall, striking woman in her 60’s needed disarming.

Nancy’s faith was strong, and she worked hard to help others. She established a library at First Christian Church, and a cassette tape ministry that made sermons available to those who weren’t physically able to attend services. She also loved singing in the choir, occasionally playing violin in the church orchestra. After moving her church home to First Presbyterian, she kept singing, adding her strong alto voice and determined energy to the choir. She also began visiting people on behalf of the church, in hospitals and in their homes. Her bible study, and her work there as a deacon were exceptionally important to her, and her strength and kindness helped her make lasting friendships wherever she went.

In late November of 2005, Nancy was admitted to Albany Medical Center, having shown stroke-like symptoms while visiting one of her sons for Thanksgiving. After some analysis, the neurologists determined that she had Cruetzfeldt-Jakob’s disease, an extremely rare neurodegenerative disease which is fatal within months of the onset of symptoms.

In spite of her diagnosis, Nancy continued energetically adapting to the burdens of the disease, remaining open and in good spirits through the end. In the three months of her illness, she was constantly surrounded by her family and her extensive community of friends. As we all understand the depth of her love and involvement with so many people, it’s clear that her largest knitting project is now complete – a beautiful tapestry of people connected with one another. She must be very pleased.

Nancy is preceded in death by her parents, Thompson George Marsh and Susan Raymond Marsh, and by her ex-husband Loy Banks.

She is survived by her three sisters, Alice Abbot, Lucy Marsh, and Mary Zulack, her three children, William Banks, Afton Rorvik, and Joseph Banks, and her 6 grandchildren, Ian Banks, Karl Rorvik, Stephen Banks, Robert Banks, Annalisa Rorvik, and Mark Banks.


My heartfelt sympathy to the family of Nancy. Although I did not know her I especially feel your loss today because my 48 year old brother also passed from CJD 11 years ago. That was the 1st time I had heard of the disease. I too share a love of knitting. My prayers are with you all.

Jana Skradski Jan 27, 2006 Fort Collins, CO

Fort Collins, CO

Population 2000: 118,652

Metro area: Fort Collins-Loveland

Colorado — Population: 4,301,261 ; 24th, 12/00
According to http://www.50states.com/colorado.htm


did she consume venison?

did she have surgery, where others that have consumed venison, that might have been exposed to CWD had surgery?

did she donate blood?

how many have been exposed via the surgical/medical arena by CWD in this area?




Subject: Prions in Skeletal Muscles of Deer with Chronic Wasting Disease [SCIENCE FULL TEXT]
Date: January 26, 2006 at 12:23 pm PST

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease

Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§

1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA.

*These authors contributed equally to this work.

†Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA.

‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland.

§To whom correspondence should be addressed: E-mail: [email protected]

Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD.

To test whether skeletal muscle of diseased cervids contained prion infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein (CerPrP), were inoculated intracerebrally with extracts prepared from the semitendinosus/semimembranosus muscle group of CWD-affected mule deer or from CWD-negative deer. The availability of CNS materials also afforded direct comparisons of prion infectivity in skeletal muscle and brain. All skeletal muscle extracts from CWD-affected deer induced progressive neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times ranging between 360 and ~490 d, whereas the incubation times of prions from the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the diagnosis of prion disease was confirmed by the presence of PrPSc in the brains of multiple infected Tg(CerPrP)1536 mice (see supporting online material for examples). In contrast, skeletal muscle and brain material from CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1) and PrPSc was not detected in the brains of sacrificed asymptomatic mice as late as 523 d after inoculation (supporting online material).

Our results show that skeletal muscle as well as CNS tissue of deer with CWD contains infectious prions. Similar analyses of skeletal muscle BSE-affected cattle did not reveal high levels of prion infectivity (3). It will be important to assess the cellular location of PrPSc in muscle. Notably, while PrPSc has been detected in muscles of scrapie-affected sheep (4), previous studies failed to detect PrPSc by immunohistochemical analysis of skeletal muscle from deer with natural or experimental CWD (5, 6). Since the time of disease onset is inversely proportional to prion dose (7), the longer incubation times of prions from skeletal muscle extracts compared to matched brain samples indicated that prion titers were lower in muscle than in CNS where infectivity titers are known to reach high levels. Although possible effects of CWD strains or strain mixtures on these incubation times cannot be excluded, the variable 360 to ~490 d incubation times suggested a range of prion titers in skeletal muscles of CWD-affected deer. Muscle prion titers at the high end of the range produced the fastest incubation times that were ~30% longer than the incubation times of prions from the CNS of the same animal. Since all mice in each inoculation group developed disease, prion titers in muscle samples producing the longest incubation times were higher than the end point of the bioassay, defined as the infectious dose at which half the inoculated mice develop disease. Studies are in progress to accurately assess prion titers.

While the risk of exposure to CWD infectivity following consumption of prions in muscle is mitigated by relatively inefficient prion transmission via the oral route (8), these

results show that semitendinosus/semimembranosus muscle, which is likely to be consumed by humans, is a significant source of prion infectivity. Humans consuming or handling meat from CWD-infected deer are therefore at risk to prion exposure.

References and Notes

1. P. J. Bosque et al., Proc. Natl. Acad. Sci. U.S.A. 99, 3812 (2002).

2. S. R. Browning et al., J. Virol. 78, 13345 (2004).

3. A. Buschmann, M. H. Groschup, J. Infect. Dis. 192, 934 (2005).

4. O. Andreoletti et al., Nat. Med. 10, 591 (2004).

5. T. R. Spraker et al., Vet. Pathol. 39, 110 (2002).

6. A. N. Hamir, J. M. Miller, R. C. Cutlip, Vet. Pathol. 41, 78 (2004).

7. S. B. Prusiner et al., Biochemistry 21, 4883 (1980).

8. M. Prinz et al., Am. J. Pathol. 162, 1103 (2003).

9. This work was supported by grants from the U.S. Public Health Service 2RO1 NS040334-04 from the National Institute of Neurological Disorders and Stroke and N01-AI-25491 from the National Institute of Allergy and Infectious Diseases.

Supporting Online Material



Animal Prion Diseases Relevant to Humans (unknown types?)
Thu Oct 27, 2005 12:05

About Human Prion Diseases /
Animal Prion Diseases Relevant to Humans

Bovine Spongiform Encephalopathy (BSE) is a prion disease of cattle. Since 1986, when BSE was recognized, over 180,000 cattle in the UK have developed the disease, and approximately one to three million are likely to have been infected with the BSE agent, most of which were slaughtered for human consumption before developing signs of the disease. The origin of the first case of BSE is unknown, but the epidemic was caused by the recycling of processed waste parts of cattle, some of which were infected with the BSE agent and given to other cattle in feed. Control measures have resulted in the consistent decline of the epidemic in the UK since 1992. Infected cattle and feed exported from the UK have resulted in smaller epidemics in other European countries, where control measures were applied later.

Compelling evidence indicates that BSE can be transmitted to humans through the consumption of prion contaminated meat. BSE-infected individuals eventually develop vCJD with an incubation time believed to be on average 10 years. As of November 2004, three cases of BSE have been reported in North America. One had been imported to Canada from the UK, one was grown in Canada, and one discovered in the USA but of Canadian origin. There has been only one case of vCJD reported in the USA, but the patient most likely acquired the disease in the United Kingdom. If current control measures intended to protect public and animal health are well enforced, the cattle epidemic should be largely under control and any remaining risk to humans through beef consumption should be very small. (For more details see Smith et al. British Medical Bulletin, 66: 185. 2003.)

Chronic Wasting Disease (CWD) is a prion disease of elk and deer, both free range and in captivity. CWD is endemic in areas of Colorado, Wyoming, and Nebraska, but new foci of this disease have been detected in Nebraska, South Dakota, New Mexico, Wisconsin, Mississippi Kansas, Oklahoma, Minnesota, Montana, and Canada. Since there are an estimated 22 million elk and deer in the USA and a large number of hunters who consume elk and deer meat, there is the possibility that CWD can be transmitted from elk and deer to humans. As of November 2004, the NPDPSC has examined 26 hunters with a suspected prion disease. However, all of them appeared to have either typical sporadic or familial forms of the disease. The NPDPSC coordinates with the Centers for Disease Control and state health departments to monitor cases from CWD-endemic areas. Furthermore, it is doing experimental research on CWD transmissibility using animal models. (For details see Sigurdson et al. British Medical Bulletin. 66: 199. 2003 and Belay et al. Emerging Infectious Diseases. 10(6): 977. 2004.)


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is with a human TSE surveillance system that is terrible flawed. in 1997 cases of the _reported_ cases of cjd were at 54, to 163 _reported_ cases in 2004. see stats here;

p.s. please note the 47 PENDING CASES to Sept. 2005

p.s. please note the 2005 Prion D. total 120(8) 8=includes 51 type pending, 1 TYPE UNKNOWN ???

p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???

p.s. please note 2004 prion disease (6) 6=7 TYPE UNKNOWN???



AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.







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Well-known member
Sep 3, 2005
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Materials and Methods

Fig. S1

21 November 2005; accepted 13 January 2006 Published online 26 January 2006; 10.1126/science.1122864 Include this information when citing this paper.

Table 1. Incubation times following inoculation of Tg(CerPrP)1536 mice with prions from skeletal muscle and brain samples of CWD-affected deer.

Inocula Incubation time, mean d ± SEM (n/n0)*

Skeletal muscle Brain

CWD-affected deer

H92 360 ± 2 d (6/6) 283 ± 7 d (6/6)

33968 367 ± 9 d (8/8) 278 ± 11 d (6/6)

5941 427 ± 18 d (7/7)

D10 483 ± 8 d (8/8) 231 ± 17 d (7/7)

D08 492 ± 4 d (7/7)

Averages 426 d 264 d

Non-diseased deer

FPS 6.98 >523 d (0/6)

FPS 9.98 >454 d (0/7) >454 d (0/6)

None >490 d (0/6)

PBS >589 d (0/5)

*The number of mice developing prion disease divided by the original number of inoculated mice is shown in parentheses. Mice dying of intercurrent illnesses were excluded.



Supporting Online Material for

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease

Rachel C. Angers, Shawn R. Browning, Tanya S. Seward, Christina J. Sigurdson,

Michael W. Miller, Edward A. Hoover, Glenn C. Telling§

§To whom correspondence should be addressed: E-mail: [email protected]

Published 26 January 2006 on Science Express

DOI: 10.1126/science.1122864

This PDF file includes:

Materials and Methods

Fig. S1

Supporting Online Materials

Materials and Methods

Homogenates of semitendinosus/semimembranosus muscle (10% w/v in phosphate

buffered saline) were prepared from five emaciated and somnolent mule deer, naturally

infected with CWD at the Colorado Division of Wildlife, Wildlife Research Center.

These deer were identified as D10, D08, 33968, H92, and 5941. CWD infection was

confirmed in all cases by the presence of histologic lesions in the brain including

spongiform degeneration of the perikaryon, the immunohistochemical detection of

disease-associated PrP in brain and tonsil, or by immunoblotting of protease-resistant,

disease associated PrP (CerPrPSc). Semitendinosus/semimembranosus muscle was also

obtained from two asymptomatic, mock inoculated deer, referred to as FPS 6.68 and 9.98,

that originated from a CWD non-endemic area and which were held indoors at Colorado

State University from ten days of age. These control deer were confirmed negative for

CWD by histopathological and immunohistochemical analysis of brain tissue at autopsy.

The utmost care was taken to avoid inclusion of obvious nervous tissue when muscle

biopsies were prepared and to ensure that contamination of skeletal muscle samples with

CNS tissue did not occur. Fresh, single-use instruments were used to collect each sample

biopsy and a central piece from each sample was prepared with fresh, disposable

instruments to further isolate muscle tissue for inoculum preparation. Brain samples for

transmission were prepared separately from muscle as additional insurance against cross



Groups of anesthetized Tg(CerPrP)1536 mice were inoculated intracerebrally with 30 µl

of 1 % skeletal muscle or brain extracts prepared in phosphate buffered saline (PBS).

Inoculated Tg(CerPrP) mice were diagnosed with prion disease following the progressive

development of at least three neurologic symptoms including truncal ataxia, ‘plastic’ tail,

loss of extensor reflex, difficultly righting, and slowed movement. The time from

inoculation to the onset of clinical signs is referred to as the incubation time.

For PrP analysis in brain extracts of Tg(CerPrP)1536 mice, 10 % homogenates prepared

in PBS were either untreated (-) or treated (+) with 40 µg/ml proteinase K (PK) for one

hour at 37oC in the presence of 2% sarkosyl. Proteins were separated by sodium dodecyl

sulfate polyacrylamide gel electrophoresis, analyzed by immunoblotting using anti PrP

monoclonal antibody 6H4 (Prionics AG, Switzerland), incubated with appropriate

secondary antibody, developed using ECL-plus detection (Amersham), and analyzed

using a FLA-5000 scanner (Fuji).


Fig. S1

PrP in brain extracts from representative Tg(CerPrP)1536 mice receiving muscle or CNS

tissue inocula from CWD-affected or CWD-negative deer. Extracts were either treated

(+) or untreated (-) with proteinase K (PK) as indicated. The positions of protein

molecular weight markers at 21.3, 28.7, 33.5 kDa (from bottom to top) are shown to the

left of the immunoblot.




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Well-known member
Feb 10, 2005
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Montana is cwd free, so far, so article is wrong on that account.


Well-known member
Sep 3, 2005
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now, the next questions is how many animals did they expose???




Q: Where has CWD been found in Montana?

A: CWD has not been found in Montana's wild deer and elk populations. However, in June 1998 and again in June 1999, elk shipped to Oklahoma from an alternative livestock facility near Philipsburg were confirmed to have CWD. In November and December 1999, 83 elk at the Philipsburg facility were destroyed. Nine of the destroyed elk later tested positive for CWD.


Q: What kind of testing and surveillance is in place in Montana on native deer and elk, and on alternative livestock farms and what are the results?

A: FWP has conducted statewide sampling of wild deer and elk for CWD since 1998, with approximately 7,000 animals taken by hunters showing no CWD infections. Since 2002, FWP has concentrated sampling efforts in northeastern and southeastern Montana along borders with states and provinces where CWD is known to occur. FWP also tests elk and deer that display clinical symptoms that suggest CWD and none of these animals has tested positive. Old age, other diseases and chronic malnutrition can result in symptoms similar to CWD.

Any animal that dies on a licensed alternative livestock facility in Montana must be tested for CWD by law. Nearly 3,500 animals to date have tested negative for CWD. The only positive animals found were the nine that tested positive at the Philipsburg alternative livestock facility.




flounder said:

now, the next questions is how many animals did they expose???




Q: Where has CWD been found in Montana?

A: CWD has not been found in Montana's wild deer and elk populations. However, in June 1998 and again in June 1999, elk shipped to Oklahoma from an alternative livestock facility near Philipsburg were confirmed to have CWD. In November and December 1999, 83 elk at the Philipsburg facility were destroyed. Nine of the destroyed elk later tested positive for CWD.


Q: What kind of testing and surveillance is in place in Montana on native deer and elk, and on alternative livestock farms and what are the results?

A: FWP has conducted statewide sampling of wild deer and elk for CWD since 1998, with approximately 7,000 animals taken by hunters showing no CWD infections. Since 2002, FWP has concentrated sampling efforts in northeastern and southeastern Montana along borders with states and provinces where CWD is known to occur. FWP also tests elk and deer that display clinical symptoms that suggest CWD and none of these animals has tested positive. Old age, other diseases and chronic malnutrition can result in symptoms similar to CWD.

Any animal that dies on a licensed alternative livestock facility in Montana must be tested for CWD by law. Nearly 3,500 animals to date have tested negative for CWD. The only positive animals found were the nine that tested positive at the Philipsburg alternative livestock facility.



And that is one of the reasons Game Farms are outlawed in Montana...

There was just an article in yesterdays Great Falls Tribune where the Fish and Game stated they had completed testing again this year without finding any cases in the WILD herd...They consider the wild herd to be "CWD free" for now anyway....


Well-known member
Jul 27, 2005
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Alberta Canada
Didn't know game farms in Montana were outlawed!! Right on the way it should be everywhere!!! Alberta allows game farms now we're having problams with farms goin under and these"ranchers "lettin thier animals go into the wild....not legally but its happenin


Well-known member
Sep 3, 2005
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have you heard of the the 'hole in the fence gang' ;-(

check out the infection rate of this farm, and how many they could not find?

i pray that cwd is not infectious to cattle via casual contact, environment, etc, much less all the tissues from road kill deer over the years in feed for cattle. only time will tell, too early to tell now. the continous rendering at low temps due to the oil crunch in the late 70s early 80s, the technology was shipped from the USA to the UK and the UK used it for some 5 years before we did, so they had some 5 year jump with the agent. please dont ask me to find that document, but it's there somewhere in my files.

again, most important here, look at the damn infection rate, of the deer they did test, the rest went missing in the wild... very disturbing... tss

##################### Bovine Spongiform Encephalopathy #####################

Subject: HOLE IN THE FENCE MAD DEER MAKE GREAT ESCAPE TO INFECT OTHERS (who is the hole in the fence gang?)
Date: January 21, 2006 at 2:04 pm PST
Wildlife officials find only 4 deer on infected game farm

PLOVER, Wis. Sharpshooters killed only four deer at a central Wisconsin game preserve where a number of animals were found to have chronic wasting disease.

State officials had expected to find as many as 40 deer there.

They plan to meet with the preserve's owner for clues as to why so few deer were found in an enclosure where a hole found in a fence prompted concern that some deer escaped.

Sharpshooters had killed 76 deer in breeding pens on Tuesday and four additional deer about a week ago.

Authorities, though, were especially interested in the 40 or so bucks they believed were at Stan Hall's shooting preserve near Plover.

Before sharpshooters arrived, 20 of Hall's deer tested positive for chronic wasting disease.

Copyright 2006 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.


Posted January 18, 2006

State kills CWD-infected herds at Almond preserve

Eradication planned before recent breach in fence

By Heather Clark
Journal staff

ALMOND -- An Almond deer hunting preserve under watch for having deer test positive for chronic wasting disease in the past is being eradicated.

State officials began the task of killing the breeding and hunting herds at Buckhorn Flats, 9403 Third St., on Tuesday, closing off neighboring roads for safety purposes during the shootings.

The Portage County Sheriff's Department was called out about 6 a.m. Tuesday at the request of the state Department of Agriculture, Trade and Consumer Protection (DATCP) to block off Second Avenue from Third Street to Highway J as a safety measure during the shootings, officials said.

The roads were re-opened to through traffic just before 11 a.m.

The killings were planned prior to the recent concern that diseased deer escaped the preserve.

Preserve owner Stan Hill discovered the fence had been cut open and food placed near the opening to bait the deer. When notified, the DATCP closed off the opening and the state Department of Natural Resources was called in. About 40 deer had been known to roam the 59 acres of fenced-in preserve.

Portage County Sher-iff's Department's investigation into that criminal damage continues.

DNR sharpshooters and other personnel remained on site until Monday afternoon, having laid bait for deer near the damaged area of the fence. During that time, four deer were killed coming back to the fenced area, said Alan Crossley, the DNR's chronic wasting disease project leader.

The group left when the DATCP said it was arriving for the scheduled eradication, and Crossley was not sure when they would return.

"Whether those are deer from inside the pen is going to be hard to know, but we felt that was the first place that made the most sense for us to set up and shoot," he said, adding that samples from those two does and two fawns are in the process of being tested.

"The remaining question is OK, is there anything we should do in the short term to try to get additional samples, and that would likely involve working with local landowners," he said.

Hill had been fighting a July 2003 order that the livestock be killed after deer from the preserve were found to have the disease. An agreement between Hill and the state and federal agriculture agencies was reached in December.

Hill's property is about 70 acres, 59 of which are in the fenced-in preserve and another fenced portion contains a breeding herd.

The breeding herd, which was closed off in a different but nearby pen, was comprised of 79 does, fawns and yearling bucks at Hill's last count. DATCP found three dead when they arrived Tuesday, which is not uncommon, said Donna Gilson, communication specialist with the state DATCP. They killed the remaining 76. The carcasses have been transported to the state's testing facility, where samples will be sent to Iowa for CWD testing. Results will take about three weeks, she said.

"We will have people in and out for the next several days," Gilson said. "Killing the hunting preserve herd is a much more complex operation because they are over a larger area, so that will take some time."

The DNR had been surveying wild deer through hunter registration in the past, and given the recent preserve breach, that likely will continue, Crossley said. But should the decision be made to continue killing wild deer outside of the preserve, it would be done in agreement with individual neighboring property owners, he said.

The killings over the weekend were set up on a neighboring property with that landowner's permission, he said.

Hill will be paid up to a maximum of $4,500 per animal from state and federal funds, Gilson said.



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Aug 26, 2005
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It seems that the predators, if susceptable, would get the same disease. Is this showing up in predators? Maybe carnivores have something in them that does not allow them to get the disease. I have no idea here, I am just guessing. If this is the case, carnivores could play a very important role in reducing the spread of the disease.

I know my dog can eat some stuff that is pretty nasty and not get sick.


Well-known member
Feb 10, 2005
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Montgomery, Al
Species barriers are evident.

Supposedly the human species barrier for vCJD is the reason for such few cases.

Ruminants seem to be especially susceptible to TSE's.


Well-known member
Sep 3, 2005
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kathy asks;

> flounder, explain how lowering the temperature of the rendering caused an increase in the

> "infectious" nature of the MBM??

another one of kathys' trick questions ???

either way, maybe some might find interest in this;

According to USDA’s Animal and Plant Health Inspection Service (APHIS), if a TSE agent is

present in a rendered product, the continuous rendering process most used in the United States

will only reduce infectivity by two logs or less, while batch rendering will reduce infectivity by

three logs. Because the BSE agent may survive the rendering process, potentially high risk

material from cattle over 12 months should not be recycled to humans through the rendering

process. ...............

In reading your short article about 'Scientist warn of CJD epidemic'
news in brief Jan. 1, 2000. I find the findings in the PNAS old news,
made famous again. Why is the U.S. still sitting on their butts,
ignoring the facts? We have the beginning of a CJD epidemic in the
U.S., and the U.S. Gov. is doing everything in it's power to conceal

The exact same recipe for B.S.E. existed in the U.S. for years and
years. In reading over the Qualitative Analysis of BSE Risk Factors-1,
this is a 25 page report by the USDA:APHIS:VS. It could have been done
in one page.
The first page, fourth paragraph says it all;

"Similarities exist in the two countries usage of continuous rendering
technology and the lack of usage of solvents, however, large differences
still remain with other risk factors which greatly reduce the potential
risk at the national level."

Then, the next 24 pages tries to down-play the high risks of B.S.E. in
the U.S., with nothing more than the cattle to sheep ratio count, and
the geographical locations of herds and flocks. That's all the evidence
they can come up with, in the next 24 pages.

Something else I find odd, page 16;

"In the United Kingdom there is much concern for a specific continuous
rendering technology which uses lower temperatures and accounts for 25
percent of total output. This technology was _originally_ designed and
imported from the United States. However, the specific application in
the production process is _believed_ to be different in the two

A few more factors to consider, page 15;

"Figure 26 compares animal protein production for the two countries.
The calculations are based on slaughter numbers, fallen stock estimates,
and product yield coefficients. This approach is used due to variation
of up to 80 percent from different reported sources. At 3.6 million
tons, the United States produces 8 times more animal rendered product
than the United Kingdom."

"The risk of introducing the BSE agent through sheep meat and bone meal
is more acute in both relative and absolute terms in the United Kingdom
(Figures 27 and 28). Note that sheep meat and bone meal accounts for 14
percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent
or 22 thousand tons in the United States. For sheep greater than 1 year,
this is less than one-tenth of one percent of the United States supply."

"The potential risk of amplification of the BSE agent through cattle
meat and bone meal is much greater in the United States where it
accounts for 59 percent of total product or almost 5 times more than
the total amount of rendered product in the United Kingdom."

Considering, it would only take _one_ scrapie infected sheep to
contaminate the feed. Considering Scrapie has run rampant in the U.S.
for years, as of Aug. 1999, 950 scrapie infected flocks.
Also, Considering only one quarter spoonful of scrapie infected
material is lethal to a cow. Considering all this, the sheep to cow
ratio is meaningless. As I said, it's 24 pages of B.S.e.

To be continued...

Terry S. Singeltary Sr.




The following are the main conclusions drawn by the BSE Inquiry from the scientific study of

the BSE epidemic1:

1. The vector responsible for the epidemic of BSE in cattle was MBM

The spread of BSE in cattle to the point where it became an epidemic came about from the

use of meat and bone meal in cattle feed. The MBM in question was infective because it had

been made by rendering infective offal from cattle suffering from or merely incubating the

disease. As little as a gram of this material could cause death if ingested by other cattle. It

was so infective that accidental contamination of cattle feed with pig or poultry feed

containing MBM was a significant factor which continued to spread BSE after the ban on the

use of MBM in cattle feed. Apart from MBM in feed, transmission from mother to calf is

likely to have played a part. We cannot yet say whether contamination of pastures played a

part. The suggestion has been made that the BSE agent may have been spread in the early

stages in hormones or other bovine material used in veterinary preparations. This possibility

cannot be discounted. But the overwhelming vector of the epidemic was MBM in cattle feed.

2. The unmodified scrapie agents were not the agents responsible for BSE

While it was reasonable in February 1989 to accept the hypothesis that the cases of BSE

being reported had come about through the rendering of carcasses of sheep infected with

extant strains of scrapie established in the national flock, this is no longer plausible. We

think it likely that the passive surveillance system failed to detect several cycles of BSE in the

South West of England in the 1970s and early 1980s. Each cycle was followed by more

extensive contamination of MBM. Much of the recycling could not be detected because

tissues from animals incubating the disease but not showing signs were involved; but it is

likely that there were isolated animals which did develop signs and were slaughtered or died

of the disease. BSE was unknown at the time and it seems possible that the disease in such

cattle, sometimes called ‘downer’ cattle, might have been ascribed to known disorders such as

hypomagnesaemia. These early cycles began because a novel TSE agent originated in the

early 1970s. The cause of this novel agent is likely to have been a new prion mutation in

cattle, or possibly sheep. Moreover, other mammalian species whose carcass waste was

included in MBM cannot be excluded. It is conceivable that the conversion of normal prion

protein into its infective form was initiated not by a gene mutation, but by an environmental

agent, such as a toxic chemical, although this has not yet been achieved experimentally. It is

now not possible to be sure which of the hypotheses as to the origin of the novel agent is

correct. Current knowledge suggests that the original agent was not the unmodified scrapie

agent or agents. We have also noted a number of pointers which could have led to the

conclusion by mid-1990, and certainly well before 20 March 1996, that the agent fuelling the

BSE epidemic was not then (if it ever had been) the unmodified scrapie agent or agents.

3. Changes in rendering

It is a common misconception that reduction in temperature or a failure to prescribe minimum

holding times in the rendering of carcass waste led to failure of inactivation of the scrapie

1 Inquiry, Volume 2 paragraph 7.3 and Volume 1 paragraphs 1123-1124


agent and transmission across the species barrier to cattle. Changes in the rendering process

in the late 1970s and early 1980s, namely the switch from batch to continuous processing and

the abandonment of solvent extraction of tallow, might have led to reduction in inactivation

of the agent in MBM, but it is now known that the processes used previously were also

incapable of completely inactivating TSE agents. No commercial rendering procedure has

been designed capable of completely inactivating BSE in MBM before or since.




1. The vector responsible for the epidemic of BSE in cattle was MBM.2

1.1 The spread of BSE in cattle to the point where it became an epidemic came about from

the use of meat and bone meal in cattle feed.


No experiments have been conducted in which cattle were fed MBM infected with BSE under

controlled conditions to show, unequivocally, that MBM can act as the vector of BSE (see

Appendix 1.1.4). However, three sets of evidence support the view that MBM acts as the

vector of this disease:

Consumption of cattle concentrates containing MBM was the only common factor

detected amongst all BSE cases in the initial epidemiological study (see Appendix 1.1.1).

This result would be even more compelling if it had been shown that the consumption of

these concentrates did not occur, or was less in BSE free cattle.

Dairy herds have much greater disease incidence than beef suckler herds. In cattle used

for milk production (dairy herds), calves are removed from their mother shortly after birth

and reared artificially on proprietary feeds. In beef suckler herds, calves suckled by their

mothers normally receive only milk and forage (grass, hay) in the first weeks of life.

Calves born in the year after the 1988 ruminant feed ban were three times less likely to

develop BSE than calves born in the year prior to the ban. Furthermore, only two affected

animals have so far been identified that were born after the more substantial ban of 1996

which prohibited the use of mammalian MBM in all feed for farmed animals (see

Appendices 1.1.2, especially Table II, and 1.1.3).

Calf feeding practices peculiar to the UK in the 1970s and 1980s may shed new light on the

otherwise puzzling fact of the time and place of the origin of this epidemic. MBM had

regularly been incorporated into compound feeds for adult cattle (especially dairy cows) both

in Europe and the USA for at least half of the twentieth century (Cooke, 1998). Thus, for

many years, in UK and many other countries (eg USA and continental Europe) dairy cattle

were fed protein supplements that contained MBM for the first time at the start of their first

lactation, when they were between two and two and a half years of age. However,

epidemiological evidence suggests that the majority of cows become infected by BSE when

they are calves (Wilesmith et al., 1988; Donnelly and Ferguson, 2000; see also Appendices

1.1.5 and 1.1.6). During the 1970s feed compounders in the UK began to introduce MBM

into the high protein pelleted rations fed to artificially-reared calves from the dairy herd,

typically beginning in the first two weeks of life (Webster, 1984). In contrast, elsewhere in

Europe and in the USA, it appears that little or no MBM was fed to young calves (see

Appendices 1.1.5 and 1.1.6). However, in Australia MBM was used in calf starter rations

during the period 1970s to the late 1980s. Australia is scrapie free (see Appendix 2.4.1).

1 Volume 2, paragraph 7.3 and Volume 1, paragraphs 1123 and 1124

2 Italicised headings are statements made in the Report of the BSE Inquiry


These considerations imply that the UK was the only country, in which scrapie was endemic,

where significant amounts of MBM were fed to very young calves and this practice began in

the 1970s.

The evidence outlined in this section taken together suggests that cattle may be more

susceptible to BSE in the early weeks of their lives. This suggestion is testable by


1.2 The MBM in question was infective because it had been made by rendering infective offal

from cattle suffering from or merely incubating the disease.


This conclusion is supported by the evidence that raw brain from BSE affected cows infects

cows and mice when administered by mouth or by injection. Furthermore, rendered brain

from BSE affected cows infects mice when delivered by injection. From these observations it

is reasonable to infer that this brain material, contained in MBM, was also infectious when

fed to cows (see Appendix 1.2).

1.3 As little as a gram of this material could cause death if ingested by other cattle.


Agreed. Seven out of ten calves that were fed 1 gram of brain from BSE cases developed

BSE. The remaining animals were culled in March 2001. The brainstem of each of these

animals has been subjected to detailed examination and no sign of BSE infection was

observed in this brain region (S Hawkins, personal communication). An experiment is in

progress using oral doses of 1g to 0.00lg. None of the animals have yet been culled and it is

likely to be several years before the results of these experiments are known.

1.4 It was so infective that accidental contamination of cattle feed with pig or poultry feed

containing MBM was a significant factor which continued to spread BSE after the ban on

the use of MBM in cattle feed.


This conclusion of the Inquiry is very strongly supported by the success of the various feed

bans in slowing the spread of infection. The cohort of calves born after the 1990 specified

bovine offal ban were about half as likely to develop BSE as the cohort of calves born in the

year leading up to the ban, and continued at a low level (Stevenson, 2000) (see Appendices

1.1.2 Table II, and 1.1.3).

The Eastern part of Britain had more cases of BSE in cows born after the 1988 ban than other

regions. This is a part of Britain with a large number of pig and poultry farms where the

chance of cross contamination of feed was higher than in other regions (see Appendix 1.4). It

is also possible that pastures may have been contaminated by slurry from pigs and poultry fed

MBM (see Response 1.6 below).

1.5 Apart from MBM in feed, transmission from mother to calf is likely to have played a part.



However, the Inquiry also expressed the view that the role of maternal transmission in the

spread of BSE ‘remains uncertain’ (Volume 2 paragraph 3.117). There is indeed some reason

to doubt conclusion 1.5. As noted in the Inquiry document (Volume 2 paragraphs 3.106-

3.108), the evidence in support of transmission from mother to calf comes from a study in

which all calves were potentially exposed to infected feed. The offspring of BSE infected

dams were more commonly affected by BSE than the offspring of BSE free dams. After

independent analysis by several research groups, a consensus figure of up to 10% maternal

transmission was used. The interpretation of this result is, however, not straightforward. The

offspring of infected dams might have inherited susceptibility for BSE or they might, indeed,

have been infected by their mother. More recently, the small number of cows infected with

BSE born after the comprehensive feed ban of 1996 shed doubt upon the figure of 10%. If

maternal transmission is this common, more cases would be expected to occur in the cohorts

currently approaching five years of age than has been observed (see Appendix 1.5).

1.6 We cannot yet say whether contamination of pastures played a part............


6. Alternative Theories

6.1 The organophosphate theory (Volume 1, paragraph 1123)

The theory that BSE was caused by a reaction to the use of organophosphorus compounds

(OPs) poured on cattle as systemic pesticides cannot be reconciled with the epidemiology and

is not supported by research. One experiment has, however, given some limited support to

the possibility that the OP Phosmet might modify the susceptibility of cells to the prion

disease agent.


See Appendices and 4.8.1, last paragraph.

6.2 The autoimmune theory (Volume 1, paragraph 1124)

There are a number of reasons why this theory does not seem viable, including: the fact that

mouse-adapted BSE can be transmitted by intracerebral inoculation to mice lacking a

functional immune system; and the fact that the theory is incompatible with what has been

established about the central role of the prion protein in TSEs.


It is agreed that this theory is not viable. See Appendix 4.8.2, last paragraph.


5 July 2001


Rendering practices and inactivation of the TSE agents

OIE 2003


econ101 ask ;

> Is this showing up in predators?

An organism that lives by preying on other organisms.

what about a veghead that has some sort of surgery and is contaminated via the multitude of proven routes and sources via someone else that contracted an animal TSE via consumption?

what about a mouse, the mouse contract TSE.

what about sheep, i don't know if you can count them as a predator? but they get it by there non forced oral consumption, same with mink, same with cows, same with deer and elk, same with racoons, same with cats exotic and domestic, dogs too (just not documented per say due to they did not want to pursuit it, just about like the infamous atypical Vermont sheep that were so important, they put off the mouse bio assays 2+ years, and i don't know if they ever continued, thats another story not to forget). lets see, oh yes, the infamous red neck ostrich, he got a TSE too. some evidence with chickens, and we know pigs are susecpatable. primates, humans, deer, elk, sheep, all susceptable to prions orally. oh yes, and now the moose.

canine ataxia or TSE ?

GAH WELLS (very important statement here...TSS)


AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.



76 pages on hound study;


> I thought that in Britain dogs had contracted BSE, but perhaps not.

not so fast here;

The spongiform changes were not pathognomonic (ie.
conclusive proof) for prion disease, as they were atypical,
being largely present in white matter rather than grey matter in
the brain and spinal cord. However, Tony Scott, then head of
electron microscopy work on TSEs, had no doubt that these
SAFs were genuine and that these hounds therefore must have
had a scrapie-like disease. I reviewed all the sections
myself (original notes appended) and although the pathology
was not typical, I could not exclude the possibility that this was
a scrapie-like disorder, as white matter vacuolation is seen
in TSEs and Wallerian degeneration was also present in the
white matter of the hounds, another feature of scrapie.

38.I reviewed the literature on hound neuropathology, and
discovered that micrographs and descriptive neuropathology from
papers on 'hound ataxia' mirrored those in material from
Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had
done much of this work, and I obtained original sections
from hound ataxia cases from him. This enabled me provisionally to
conclude that Robert Higgins had in all probability detected
hound ataxia, but also that hound ataxia itself was possibly a
TSE. Gerald Wells confirmed in 'blind' examination of single
restricted microscopic fields that there was no distinction
between the white matter vacuolation present in BSE and
scrapie cases, and that occurring in hound ataxia and the hound
survey cases.

39.Hound ataxia had reportedly been occurring since the 1930's,
and a known risk factor for its development was the feeding
to hounds of downer cows, and particularly bovine offal.
Circumstantial evidence suggests that bovine offal may also be
causal in FSE, and TME in mink. Despite the inconclusive
nature of the neuropathology, it was clearly evident that this
putative canine spongiform encephalopathy merited further

40.The inconclusive results in hounds were never confirmed,
nor was the link with hound ataxia pursued. I telephoned Robert
Higgins six years after he first sent the slides to CVL.
I was informed that despite his submitting a yearly report to the
CVO including the suggestion that the hound work be continued,
no further work had been done since 1991. This was
surprising, to say the very least.

41.The hound work could have provided valuable evidence
that a scrapie-like agent may have been present in cattle offal long
before the BSE epidemic was recognised. The MAFF hound
survey remains unpublished.

Histopathological support to various other published
MAFF experiments

42.These included neuropathological examination of material
from experiments studying the attempted transmission of BSE to
chickens and pigs (CVL 1991) and to mice (RVC 1994).


It was thought likely that at least some, and probably all, of the cases
in zoo animals were caused by the BSE agent. Strong support for this
hypothesis came from the findings of Bruce and others (1994)
( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. &
Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and
scrapie to mice: strain variation and species barrier. Philosophical
Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405
), who demonstrated that the pattern of variation in incubation period
and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that
seen when this panel of mouse strains was inoculated with brain from
cattle with BSE. The affected zoo bovids were all from herds that were
exposed to feeds that were likely to have contained contaminated
ruminant-derived protein and the zoo felids had been exposed, if only
occasionally in some cases, to tissues from cattle unfit for human



i wrote DEFRA about this study ;


Department for Environment,
Food & Rural Affairs

Area 307, London, SW1P 4PQ
Telephone: 0207 904 6000
Direct line: 0207 904 6287
E-mail: h.mcdonagh.defra.gsi.gov.uk


Mr T S Singeltary
P.O. Box 42
USA 77518

21 November 2001

Dear Mr Singeltary TSE IN HOUNDS

Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

critical. For more details see-


As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

I hope this is helpful

Yours sincerely 4


BSE; and other TSEs

There are a number of Transmissible Spongiform Encephalopathies (TSEs) affecting animals and man which are caused by unconventional infectious agents. The individual agents responsible for specific TSEs have not been completely characterised, although their overall composition appear to be very similar.

Human spongiform encephalopathies
Kuru, Creutzfeldt-Jakob Disease (CJD) and its more rare variant, Fatal Familial Insomnia and Gerstmann-Sträussler-Scheinker (GSS) disease, are examples of spongiform encephalopathies found in man. Like the animal disorders, they are progressive and universally fatal. Kuru at one time was common in certain tribes in Papua New Guinea although not seen elsewhere. Transfer of infection was thought to occur through ceremonial handling and ingestion of human brains affected by the disease. As the disease is not maternally transmitted, the incidence of kuru has decreased dramatically since these practices ceased around 1956. Several cases do still occur each year in patients over thirty years of age; this is consistent with an incubation period of 30 years or more.

CJD is a rare disease of man which affects about one person per million each year and is prevalent worldwide.

Animal spongiform encephalopathies
Perhaps the most widely recognised spongiform encephalopathy of animals is scrapie which is a fatal progressive neurological disorder of sheep. Scrapie has been reported in many countries and has been recognised in British sheep flocks for over two centuries, having been first recorded in 1732. Scrapie affects sheep and goats naturally and can be transmitted experimentally to several animal species.

Bovine spongiform encephalopathy (BSE) was recognised as a potential member of the scrapie family of diseases as soon as it was discovered in November 1986. It showed all of the pathological characteristics of a TSE.

Similar TSEs have been found to occur in other species [see below].

Apart from scrapie, before the first identification of BSE two other "naturally occurring" TSEs were identified in mink, and in deer and elk. In addition, there have been clusters of TSE cases in felines and exotic zoo ruminants which appear to be related to BSE.

Transmissible Mink Encephalopathy (TME)
TME is rare, and has largely been confined to the United States of America, although incidents have also occurred in Canada, Finland, East Germany and Russia. The last outbreak was in the USA in 1985, after an outbreak free period of 22 years.

TME takes the form of a rapidly evolving epidemic, usually involving single mink farms, and appears not to spread from mother to offspring. The disease is fatal, with neurological symptoms including locomotor incoordination, somnolence and debilitation. It appears to be associated with the feeding of contaminated food. Most mink are fed on either commercially produced compound food and/or tissues of animals that have died on neighbouring farms. It had always been assumed that the most likely source of infection was scrapie in sheep fed to them.

Since BSE was first recognised there has been debate as to whether or not one American outbreak may have been caused by the feeding of cow tissue rather than sheep. Anecdotal evidence suggests that one farmer did not feed sheep to his mink, which later developed TME. If this is so, it is argued that cases of BSE may actually occur in the USA, although to date only one case has been reported (in December 2003).

Supporters of the prion theory believe that spontaneous disease may arise in any species that has a PrP gene, even in the absence of recycling of contaminated feed. The theoretical prevalence rate for this is estimated at about one per million population, the rate at which CJD occurs sporadically in humans. It is thought that if a cow affected with spontaneous BSE was fed to mink it could have caused TME.

In scientific experiments brain tissue from British BSE cases have been inoculated into mink, and in a separate experiment fed to them. Although the mink were killed by the resulting disease, the symptoms and pathology produced were not however identical to TME.

Reference: Marsh R. F and Hadlow. W. J. 1992. Transmissible mink encephalopathy. Rev.sci.tech. Off. int. Epiz. 11 (2). 539-550.

Chronic Wasting Disease (CWD)
CWD is a rare disease of elk, mule deer, black tailed deer and mule-white tailed deer crosses in the USA. There have been one or two cases elsewhere, possibly linked to American infection. Although most of the cases have occurred in captive populations, many of the animals were originally caught in the wild and are reported not to have been fed ruminant protein. Cases have been identified in wild animals too, so it must be presumed to be a natural disease rather than one introduced through feed. The name of the disease is appropriate in that the animals show progressive wasting rather than the neurological signs seen with BSE. The wasting may however be partly due to interference with brain centres that control rumination, which are also affected in BSE.


Williams E. S and Young. S. 1992. Spongiform encephalopathies in Cervidae. Rev.sci.tech. Off. int. Epiz. 11 (2). 551-567

Spraker T. R. et al 1997. Spongiform encephalopathy in free-ranging mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (cervus elaphus nelsoni) in Northcentral Colorado. Journal of Wildlife Diseases. 33 (1). 1-6.

Feline Spongiform Encephalopathy (FSE)
FSE was first identified in Britain in 1990. Since then there have been 87 cases in Great Britain, one in Northern Ireland, one in Norway and one in Liechtenstein. FSE is not an easy disease to study. Although Britain has a large cat population they would not normally have been subjected to close neurological examination in the past. Nevertheless, sufficient numbers of FSE cases have been seen and investigated to permit an association with BSE to be made. Obtaining lifetime feeding history for cats is not easy, so although all have eaten foods that would be expected to contain specified bovine offals, no particular type of food can be implicated.

The epidemic in cats is often thought to be a useful model for past human exposure to BSE. The number of feline cases has declined dramatically.

As Defra has not historically held responsibility for investigating disease, other than rabies, in domestic pets, most of the information gathered about FSE in domestic cats and zoo animals has been provided through the good will of owners and veterinary practitioners. Laboratory diagnosis of a spongiform encephalopathy in any species has however been notifiable since November 1994, thus ensuring that cases would not be missed.

Interestingly, when brain tissue from some of the early cats identified as having FSE, was inoculated into mice, the pattern of incubation periods and lesion profiles in the mice was indistinguishable from that produced by BSE.

In exotic cats there have now been nine cases in cheetahs (three were diagnosed abroad but originated in Britain), three in pumas, three in ocelots, two in tigers and two in lions.

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.


Zanusso-G, Nardelli-E Rosati-A Fabrizi-G-M Ferrari-S Carteri-A Desimone-F Rizutto-N Monaco-S. Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. LANCET, 1998 V352, N9134, OCT 3, Pp 1116-1117.

Pearson G. R. et al. 1992. Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.

Wyatt. J. M. et al. 1991. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

Gruffydd-Jones T. J. et al. 1991. Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.

Willoughby K. 1992. Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.

Exotic ruminants
For completion it is worth mentioning cases that occurred in British zoos in exotic ruminants, largely antelopes but including two Ankole cattle and one American bison. The antelopes affected are kudu (6), eland (6), arabian oryx (1), scimitar horned oryx (1), nyala (1) and gemsbok (1). With hindsight the nyala was actually diagnosed before the first case of BSE was identified but had no association with farm animals at the time.

All the exotic ruminants appear to be linked to the BSE epidemic via the consumption of contaminated feed. Although there was speculation that the kudu cases might provide evidence of horizontal transmission, this is now considered unlikely. Maternal Transmission may have occurred in one case. Kudu appeared to be particularly susceptible to BSE, being affected at a younger age than cattle, and with short clinical histories. The incompleteness of the ruminant feed ban was not appreciated at the time that the theory of horizontal transmission was being postulated.

Reference: Kirkwood J. K. and Cunningham A.A. Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record. 135. 296-303.

Page last modified: 11 August 2004


> Supposedly the human species barrier for vCJD is the reason for such few cases.

the UKBSEnvCJD only theory WILL FALL, you can take that to the bank. ...TSS


Well-known member
Jul 1, 2005
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Edmonton, Alberta, Canada
I have long argued that CWD, like all other forms of prion disease, is extremely lethal to humans and can jump the species barrier. The hypothesis put forward by people such as the chief vet here in Alberta, Dr. G. Ollis and others like Dr. Margo Pybus, that CWD does NOT pose a threat to us humans was challenged by myself and others who completely disagreed with their "hide and seek" approach to this problem. CWD is rearing its ugly head in Alberta now more than ever and will continue to do so and most certainly will find its was into the human food chain as it has already done so simply by the sheer weight of hunting stats in the region where it is most prevalent. We have to consider CWD significant threat not only to the wild animal population but to us also. Species barriers will fall to this and other dieseases.


Well-known member
Jul 1, 2005
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Edmonton, Alberta, Canada
CWD is one of those awful little diseases that falls into the "Lost" file with government employed vets and it is usually due to lame internal political doctrines that manifest their typical government responses to serious questions. I have the utmost respect for those vets who practice their profession in their field and do not profess to know all there is to know about prion diseases and the inherent known and unknown aspects of TSE diseases. Having said that, I have nothing but contempt for those who speak to serious questions posed regarding prion diseases without having any acquired knowledge that comes from years of study and bench work in the field of prion research. These people, in the employ of government agencies, tend to speak as if they are the last word on the issue and that is what is currently happening here in Alberta. Those individuals, employed as knowledgeable and well educated people working within the government framework, have little or no knowledge of prion disease and yet they put themselves forward as the official and government approved voice on what is and what is not when it comes to discussions relating to prion infectivity and all related studies of the same. That in itself is what is consumately wrong within this and other countries, inthat the true scientist(s) who dedicate their entire lives to the field of prion studies/research and present solid evidence of what prion science is all about, are left out of the question-and-answer sessions because they will either make or break the government-of-the-day "politically correct" responses to the public at large. Prion disease is relatively knew to the world of science (albeit that it has been studied for years) with respect to how it is now being thrust into the public light. For many years, prion studies has occupied a relatively unknown space at the back of the lab and certainly out of the limelight, until recently when the world was forced to accept the fact that our meat and meat by-products were publically known to be at risk. Up until that point, BSE, CJD and any other potential for TSE infectivity was kept rather low key and often misdiagnosed as something other than what it was. Alzheimer Disease being a prime example. We are now faced with having to know all there is to know about PrPsc's and their related effects on humans and our food chain derived from staples such as beef. Governments who literally tell us that all is well while they scramble to make up the next excuses to fit their overall plan of attack that is, for the most part, a complete and utter waste of time and resources, as shown with the last BSE outbreak in Canada that ultimately cost the beef industry in North America approximately 7 billion dollars and for what - a single animal diagnosed with BSE. In Canada we even had our Health Minister state publicly that it was IMPOSSIBLE for any cattle under the age of 30 months to "catch" BSE. How stupid was that comment? Our own Provincial leader, Premier Klein himself stated that it would take over a million meals of infected cow brains to bring about CJD in a human being. That one was priceless but it goes to show us how governments regard the situation of prion disease. I was present at a meeting here in Edmonton in 2003 where it was stated by one well known individual who works closely with the key folks within the Government of Alberta that prior to 1987 across Canada there were over 1000 cases of suspected BSE being "looked at" within Canada and yet that was regarded as par for the course at that time and not subject to public release back then.

So what is the answer to the CWD question? To me it is simple - if we consider it to be yet another item for the government political mainstream dog and pony show then it will be considered as nothing to worry about. Consider that the government has already stated that it intends to cull a number of deer in the southern part of Alberta to combat the spread of the disease. I guess they feel that by killing perfectly healthy animals the disease will not spread!! But if we consider CWD, BSE and any other TSE to be nothing short of the next potential plague for the human race, then perhaps we can get something done about it and fast. We cannot continue to treat prion disease with the "take two pills and call me in the morning" attitude, because the problem with Prion Disease is that it will rear its ugly head long after the current politicians are long dead. That is the nature of the disease and perhaps, just perhaps, the current political position is based upon the knowledge that due to the length of the incubation period, prion diseases fall into the slot that is titled "Let the next batch of politicians worry about it!" Some may find my words somewhat radical and even cynical, but if we sit back and take this to be nothing to worry about, something horrible this way will certainly come. The only answer is to test all animals that are to enter the human food chain - and not by having some "Meat Inspector," who walks the line of hanging carcasses and literally rubber stamps them based on smell and visual looks of the meat, and before some of you argue these points, let me ask you why is it that governments do not wish to see testing of all animals happen?? I will be happy to debate that. Sorry to be so long winded but I felt the need to vent a little today.


Well-known member
Feb 14, 2005
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Calgary Alberta
BSE tester -
let me ask you why is it that governments do not wish to see testing of all animals happen??

Same reason that you and every other BSE experts focus exclusively on testing rather than research. MONEY

BSE has become the best economic opportunity in the food industry in history. Why would anyone stop now.

Don't get me wrong BSE tester, I support testing; testing to stop the madness of BSEconomics. Testing to allow fairness in the marketplace.
But please don't think that this means I support your views on "disease"etc.

If there was money available for you to do research on alternatives to the feed transmission theory BSE tester, would you apply? I realise that the bigger payoff would be to break open and be the go too guys with testing in the conventional market. But would it be enough for you to consider alternatives if the monetary benefits were similar to the benefits from presenting the accepted test? Pretty competitive world you live in BSE tester. Do you feel that you efforts and investment will be enough with the thousands of other companies chasing the same goal? How much time and effort is being put into projects like yours? Must be millions of hours and billions of dollars eh?

While the whole time, you all follow a theory of transmission, and the theory of species leap.

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